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GP block (Y3) > Week 5: Dermatology 2 (common skin conditions) > Flashcards

Week 5: Dermatology 2 (common skin conditions) Flashcards

1
Q

Emergency dermatology

A
  • Urticaria, angioedema and anaphylaxis
  • Erythema nodosum
  • Erythema multiforme
  • Steven Johnson
  • Necrotizing fasciitis
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2
Q

Skin infections

A
  • Cellulitis
  • Impetigo
  • Fungal infections
  • Folliculitis
  • Pityriasis rosea
  • Scabies
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3
Q

Skin cancer

A
  • Basal cell carcinoma
  • Squamous cell carcinoma
  • Malignant melanoma
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4
Q

Inflammatory skin conditions

A
  • Atopic eczema
  • Acne vulgaris
  • Psoriasis and different types
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5
Q

Erythema nodosum

A
  • A type of panniculitis, an inflammatory disorder affecting subcutaneous fat
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6
Q

causes of Erythema nodosum

A
  • Hypersensitise reaction of unknown cause in most patients
  • In other case:
    • Inflammatory condition
      • IBD
      • Sarcoidosis
      • TB
    • Drug
      • Amoxicillin
      • Oral contraceptive
    • Infection
      • Streptococcal
    • malignancy

more common in women

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7
Q

presentation of erythema nodosum

A
  • Bilateral tender erythematous nodules on the anterior shins (less commonly, thighs and forearms (rarely on face))
  • 3-20cm
  • Accompanied by fever and joint pain – swollen ankle most common
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8
Q

management of erythema nodosum

A
  • Treatment of underlying condition e.g. crohns, sarcoidosis, tuberculosis, throat infection
  • Anti-inflammatory drugs e.g. ibuprofen and cortisone
  • They spontaneously resolve within 8 weeks
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9
Q

Erythema multiforme (major and minor)

A
  • Hypersensitivity reaction usually triggered by infections, most commonly herpes simpelx virus (HSV)
  • Divided into major and minor forms
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10
Q

causes of erythema multiform

A
  • Usually young adults
  • Genetic tendancy
  • Triggers
    • Drugs
      • barbiturates
      • NSAIDS
      • penicillin
    • Infections
      • mycoplasma pneumonia
      • Herpes varicella-zoster
      • Dermatophyte fungal infections
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11
Q

presentation of erythema multiforme

A
  • Eruption characterised by target lesion (few to hundreds within 24 hours)
  • First seen on the back of hands/ top of feet and then spread down limb towards trunk
  • Mucous membranes may be involved
  • May have fever or chills and arthralgia
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12
Q

management of erythema multiforme

A
  • Treatment of underlying condition
  • Acute and self limiting, usually resolving without complications
  • Itching- antihistamine/corticosteroids topical
  • Eye involvement should be treated by ophthalmologist
  • Recurrent erythema multiforme usually treated with oral acyclovir for 6 months
  • Skin biopsy may need to done to exclude other conditions
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13
Q

Urticaria, angioedema and anaphylaxis

A
  • Background (also known as hives, weals, or nettle rash) is a superficial swelling of the skin (epidermis and mucous membranes) that results in a red (initially with a pale centre), raised, and intensely itchy rash.
    • Angio-oedema is a deeper form of urticaria with transient swellings of deeper dermal, subcutaneous, and submucosal tissues, often affecting the face (lips, tongue, and eyelids), genitalia, hands, or feet. For more information, see the CKS topic on Angio-oedema and anaphylaxis
    • Urticaria and angio-oedema can co-exist (in about 40% of cases), but either can occur separately
    • Consider vasculitic urticaria – if lesion remain for longer 24hs and are painful, non blanching and palpable (esp in conjunction with fever, malaise and arthralgia)
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14
Q

Causes/ risk factors of urticaria, angioedema and anaphylaxis

A

Mast cell driven disease → release histamine, leukotrienes and prostaglandins. Triggers include

  • Certain foods
  • Certain plants, animals, latex
  • Cold
  • Hot, sweaty skin e.g. emotional stress
  • Insect bite
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15
Q

presentation of urticaria and angioedema

A
  • Pruritus
  • Vascular permeability
  • Oedema
  • Rash: erythematous swelling of various shapes and sizes, classically have central pallor with erythematous flare
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16
Q

management of urticaria

A
  • Investigations not usually required unless indicated in history and exam
  • Identify underlying cause e.g. trigger factor/ new drug
  • Antihistamine e.g. cetirizine
  • If symptoms severe give prednisolone for up to 7 days
  • If inadequate response increase dose of antihistamines
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17
Q

Necrotising fasciitis

A

is a very serious bacterial infection of the soft tissue and fascia. The bacteria multiply and release toxins and enzymes that result in thrombosis in the blood vessels. The result is the destruction of the soft tissues and fascia.

3 main types

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18
Q

three types of NF

A

Type I- polymicrobial

Type II- due to hameolytic group A streptococcus and/or staphylococci MRSA

Type III (gas gangrene e.g. due to clostridium)

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19
Q

causes/risk factors of encrotizing fascitis

A
  • Most cases are of streptococcal necrotising fasciitis in young individuals
  • Opening in the skin e.g.
  • Mandibular fracture and dental infection
  • Direct contact with someone else with it
  • Risk factors
    • NSAIDs
    • Older
    • DM
    • immune suppression
    • obesity
    • drug abuse
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20
Q

presentation of NF

A
  • Early symptoms can include:
  • a small but painful cut or scratch on the skin
  • intense pain that’s out of proportion to any damage to the skin
  • a high temperature (fever) and other flu-like symptoms
    • After a few hours to days, you may develop:
      • swelling and redness in the painful area – the swelling will usually feel firm to the touch
      • diarrhoea and vomiting

dark blotches on the skin that turn into fluid-filled blisters

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21
Q

investigations for NF

A

plain X-ray or CT scan may show soft tissue gas

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22
Q

management of NF

A
  • Surgery to remove infected tissue (amputation may be required)
  • Antibiotics
    • Vancomycin IV plus clindamycin
    • Supportive treatment e.g. IV fluids
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23
Q

Pathophysiology of NF

A

The infection starts in the superficial fascia. Enzymes and proteins released by the responsible micro-organisms cause necrosis of fascial layers. Horizontal spread of infection may not be clinically apparent on the skin surface and hence diagnosis may be delayed. The infection then spreads vertically up into the skin and down into deeper structures. Thrombosis occludes the arteries and veins leading to ischaemia and necrosis of the tissues.

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24
Q

Steven Johnson syndrome background

A
  • Immune-complex-mediated hypersensitivity disorder.
  • Ranges from mild skin and mucous membrane lesions to a severe, sometimes fatal systemic illness:
    • toxic epidermal necrolysis (TEN).
    • SJS, SJS/TEN overlap and TEN form a spectrum of severe cutaneous adverse reactions (SCAR) that can be differentiated by the degree of skin and mucous membrane involvement.
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25
Q

RF for steven johnson sndrome

A

female, HIV and 10-30yo, gentic changes related to HLA

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26
Q

SJS usually caused by

A

drugs… but can also be causes by ifnections

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27
Q

drugs which cause SJS

A
  • Allopurinol
  • Carbamazepine
  • Trimethoprim
  • Abacavir
  • Phenytoin, lamotrigine
  • Sertraline
  • NSAID
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28
Q

infections which cause SJS

A
  • Viral: HSV, Epstein- barr virus, enteroviruses, HIV
  • Bacteria: Group A beta-haemolytic streptococcus, diphtheria, brucellosis, mycobacteria, Mycoplasma pneumoniae
  • Protozoal: malaria and trichomoniasis
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29
Q

presentation of SJS

A
  • Nonspecific URTI, fever, sore throat, chills, headache, muscle ache, V and D
  • Mucocutaneous lesions develop suddenly and clusters of outbreaks last from 2-4 weeks
  • Severe mucosal ulceration
  • Pt with genitourinary involvement complain of dysuria
  • Signs
    • Tachycardia, hypotension, fever, seizure, coma
    • Skin
      • Lesions occur mainly on palms, soles, forsum of hands, extensor surfaces, trunk
      • Macules  papules  vesicles  blue urticarial plaques
      • Centre of the lesion may. Be vesicular, purpuric or necrotic
      • Target
      • Lesions become bullous and rupture
      • Not pruritic
      • Nikolsky sign positive
    • Corneal ulceration
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30
Q

investigations for SJS

A
  • Investigations
    • Skin biopsy will demonstrate bullae are subepidermal
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31
Q

management of SJS

A
  • Remove causative drug
  • Intensive care may be required
  • Supportive e.g. IV fluid, pain control, lesions treated as burns
  • Topical anaesthetics, eye care
  • Treat secondary infection
  • Immunomodulation e.g. corticosteroids, DMARDS e.g. ciclosprin, anti-TNF monoclonal
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32
Q

folliculitis

A
  • Folliculitis means an inflammation or infection of the hair follicles of the skin.
  • Due to obstruction in pilosebaceous glands +- infection
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33
Q

cause sof folliculit s

A
  • Infection e.g. S.aureus, fungal e.g. Candida spp, herpetic folliculitis (HSV)
  • Immune system e.g. eosinophilic folliculitis
  • Physical irritation
  • Risk factors
    • Uncut beard
    • Shaving ‘against the grain’
    • Thick hair
    • Excessive sweating
    • Skin abrasion
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34
Q

resentation of folliculitis

A
  • It may occur as a relatively trivial irritation - superficial folliculitis, or as a more deep-seated process involving the lower hair follicle
  • Symptoms
    • Rash
    • Scratch
    • Pustule
    • Erythema if deep folliculitis
    • Regional draining of lymph nodes should be checked for adenitis  mild folliculitis
    • Folliculitis of eyelast- stye
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35
Q

management of folliculitits

A
  • Avoid precipitating factors
  • Use moisturizing shaving products
  • Shave with the grain
  • Good skin hygiene
  • Superficial – antiseptics
  • Deeper- oral antibiotics e.g. flucloxacillin, erythromycin
  • May need surgery
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36
Q

cellulitis

A
  • Acute, painful and potentially serious infection of the skin and subcutaneous tissues.
  • Infection of the dermis and subcut tissue
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37
Q

causes of cellulitis

A
  • Streptococcus or staphylococcus ( aureus) species or rarely fungal
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38
Q

RF for cellulitis

A
  • Previous cellulitis
  • Venous insuff
  • Elder
  • Alcohol dependency
  • IV drug use
  • Insect bites
  • Obesity
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39
Q

presentation of cellulitis

A
  • Poorly demarcated borders
  • Lower limb unilaterally
  • Sometimes precipitating skin lesion
  • Blisters and bullae
  • Systemic symptoms e.g. fever and mails
  • Red line streaking represents progression of infection to lymphatic system
  • Crepitus
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40
Q

investigations for cellulitis

A
  • Clinical – raised CRP, fine needle aspiration to assit diagnosis, culture fluids
41
Q

management of cellulitis

A
  • Fluclox
  • Rest and elevate
  • NSAIDS
  • Clean wound (debride)
  • Emollient
42
Q

Pityriasis rosea background

A

acute, self-limiting rash which tends to affect young adults.

43
Q

causes of pityriasis rosea

A
  • The aetiology is not fully understood but is thought that herpes hominis virus 7 (HHV-7) may play a role.
44
Q

Presentation of pityriasis rosea

A
  • minority may give a history of a recent viral infection
  • herald patch (usually on trunk)
  • a ‘fir-tree’ appearance
45
Q

management of of pityriasis rosea

A

self-limiting- disappears in 6-12 weeks

46
Q

differentiating guttate psoriasis and pityriasis rosea

A
47
Q

impetigo

A

superficial bacterial skin infection- very contagious

48
Q

causes of impetigo

A
  • Staphylococcus aureus or streptococcus pyogenes
  • Can be primary or complication of eczema, scabies or insect bites
  • Common in children
  • Spread by direct contact
49
Q

presentation of impetigo

A
  • Can be anywhere but especially found on the face, flexures and limbs
  • ‘golden’ crusted skin lesions typically found around mouth
  • Very contagious
50
Q

management of impetigo

A
  • For those not systemically unwell- hydrogen peroxide 1% cream
  • Topical fusidic acid or mupirocin
  • Extensive disease- oral flucloxacillin or erythromycin if pen allergic
  • Should be excluded from school
51
Q

Dermatophytosis (tinea) infections

A
  • Infections caused by dermatophytes
  • Invade and grow in dead keratin
  • Produce ring-like patter
  • Very common and affect diff parts of the body
52
Q

tinea infections according to site

A
53
Q

causes of tinea infecitons

A

Cause

  • Infections transmitted from person to person, from soil or animals
  • Most common organisms
    • Trichophytons rubrum
    • Trichophytons tonsurans
54
Q

presentation of tinea infections

A
  • Itching, rash and nail discolouration are the most common symptoms of tinea infection.
  • Hair loss occurs with tinea capitis (mainly a disease of children).
  • Complications such as secondary infection (cellulitis and impetigo) can lead to symptoms.
  • It is common in people who play contact sports.
  • It occurs in immunocompromised patients.
55
Q

tinea pedis

A
  • Athletes foot
  • Plantar surface- erythema, vesicles, pustules
  • Medication: miconazole (Daktarin)- oral
56
Q

tinea capitis

A

hair loss- can be scaly, crusting

57
Q

management of tinea infections

A
  • Hygiene measure
  • Antifungals
58
Q

ring worm managament

A

clostrimazole ‘ tinea corporis’

59
Q

Scabies

A

is an itchy rash caused by the parasitic mite Sarcoptes scabiei.

60
Q

causes of scabies

A
  • Spread through prolonged skin contact
  • Typically affects children and young adults
  • The scabies mite burrows into the skin, laying its eggs in the stratum corneum. The intense pruritus associated with scabies is due to a delayed-type IV hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection.
61
Q

RF for scabies

A
  • Overcrowding
  • Poverty
  • Poor nutritional status
  • Poor hygiene
  • Sexual contact
  • Immune suppression e.g HIV
  • Most common in children
62
Q

presentation of scabies

A
  • Severe pruritus worse at night
  • Close contact with people with similar symptoms
  • White lines → indicative of mite burrowing
  • Lesion may be
    • Papules
    • Vesicles
    • Pustules
    • Nodules
    • erythematous
63
Q

management of scabies

A

(everyone in household treated)

  • permethrin 5% is first-line
  • malathion 0.5% is second-line
  • pruritus persists for up to 4-6 weeks post eradication
64
Q

best -→ worse skin cancers

A

BBC→ SCC →Melanoma

65
Q

basal cell carcinoma

A
  • Most common skin cancer
  • Slow growing, locally invasive  arise from hair follicle
  • Subtypes include nodular, morphoeic, superficial and pigmented
  • Slow growing with low metastatic potential
66
Q

RF of BCC

A
  • Caucasiann (type I and II)
  • Sun exposure (UV)
  • Immunosuppression
  • Albinism
67
Q

presentation of BCC

A
  • Occurs in sun exposed sites apart from the ear
  • Early lesions are small, translucent or pearly and have raised areas with telangiectasia
  • Indurated edge and ulcerated centre
  • Slow growing but can spread deeply to cause considerable destruction
68
Q

diagnosis of BCC

A
  • Visual inspection
  • Punch biopsy if treatment other than standard surgical excision is planned
69
Q

anagement of BCC

A
  • Can be managed in primary care as long as GP trained to perform skin surgery
  • Surgical excision
  • Mohs micrographic surgery
  • Non-surgical
    • Curettage and cautery
    • Imiquimod cream
    • Radiotherapy
70
Q

squamous cell carcinoma

A
  • Malignant tumour arising from keratinising cells of the epidermis
  • Locally invasive and has the potential to metastasise
71
Q

RF for SCC

A
  • Related to sun exposure (UVR)
  • Fair skin
  • Chemical carcinogens- arsenic
  • HPV
  • Chronic inflammation
  • May arise in pre-existing solar keratoses
  • Immunosuppression after transplant
72
Q

presentation of SCC

A
  • Indurated nodular keratinising or crusted tumour that may ulcerate without evidence of keratinisation
  • Non healing ulcer or growth in one of the highest risk sun exposed area
  • Centre becomes necrotic and becomes an ulcer
  • Ulcer with hard, raised edges
  • Slow growing
  • Bleeding
73
Q

diagnosis of SCC

A

visual inspection

removal for histology

74
Q

management of SCC

A
  • Wide local excision – repeat surgery to gain adequate margins may eb required
  • Mohs’ micrographic surgery- precise technique in which excision of skin lesion is carried out in stages and checked histologically
  • Othe non-surgical procedures
    • Curettage and cautery
    • Crytotherapy
    • Imiquimod cream
    • Photodynamic therapy (PDT)
    • Electrochemotherapy
    • Radiotherapy
75
Q

melanocytes

A
  • Melanocytes are found in equal numbers in black and in white skin; however, the melanocytes in black skin produce much more melanin. People with dark brown or black skin are very much less likely to be damaged by ultraviolet (UV) radiation than those with white skin.
76
Q

non-cancerous growths of melanocytes

A
  • results in moles (benign melanocytic naevi) and freckles (ephelides and lentigines).
77
Q

most skin melanomas spread out within the epidermis…

A

If all the melanoma cells are confined to the epidermis then the lesion is a melanoma in situ, which can be cured by excision because it has no potential to spread around the body

78
Q

When the melanocytes have grown through the dermis it is known as

A

invasive melanoma → malignant melanoma

79
Q

RF for melanoma

A
  • Previous primary invasive melanoma
  • Naevi – moles
  • Sun exposure
  • Family history
80
Q

presentation of malignant melanoma

A
  • Common sites for metastases are lymph nodes, liver, lung, bone and brain. In-transit metastases are deposits from a focus of cells moving along regional lymphatic channels
    • Asymmetry.
    • Border irregular.
    • Colour irregular.
    • Diameter greater than 7 mm.
    • Evolving.
  • ABCDE
81
Q

diagnosis of melanoma

A
  • Visual inspection
  • Removal for histology
  • Staging (TNM)
82
Q

management of melanoma

A
  • Wide local excision (look for margins)
  • Vitamin D should be optimal
  • Palliative care treatment
  • Immunotherapy- ipilimumab
  • Cytotoxic chemo- dacarbazine
    *
83
Q

atopic eczema

A
  • a chronic, relapsing, inflammatory skin condition characterised by an itchy red rash that favours the skin creases such as the folds of the elbows or behind the knees
  • can become infected  crusting, weeping e.g. cellulitis
84
Q

causes of atopic eczema

A
  • Environmental irritant and allergens
    • Soaps and detergents
    • Skin infections- SA
    • Contact allergens
    • Dietary factors e.g. egg
    • Inhaled allergens e.g. dust mites
  • Genetic mutations
  • Stress
  • Hormonal changes
85
Q

Diagnosis of atopic eczema

A
  • Diagnostic
    • Itchy skin condition +
      • Itchiness in skin flexor regions
      • History of asthma or hay fever
      • General dry skin
86
Q

atopic eczema management

A
  • Education
  • Provoking factors avoided
  • Emollients form basis pf treatment (3-4 times a day)
  • Corticosteroids
    • Mild :For face and flexure (hydrocortisone)
    • Potent corticosteroid required for adults with discoid or lichenified eczema ( watch out for topical corticosteroid withdrawal)- bectamethasone
87
Q

Acne vulgaris

A
  • Acne vulgaris is a disorder of the pilosebaceous follicles found in the face and upper trunk. At puberty androgens increase the production of sebum from enlarged sebaceous glands that become blocked
    • Closed comedone- whiteheads
    • Open comedones- blackheads
    • Inflammation leads to papules, pustules and nodules
88
Q

RF for acne vulgaris

A
  • Adolescence
  • PCOS
  • Greasy substances used
  • Fx
89
Q

management of acne vulgaris

A
  • Avoid over cleaning the skin
  • Avoid oil based comedogenic skin care products
  • Wash makeup off
  • Do not pick of scratch
  • 12 week course of:
    • Topical adapalene with topicals benzoyl peroxide
    • Or topical tretinoin with topical clindamycin or doxycycline
    • COCP should be considered
    • Oral roaccutane (tretinoin)
90
Q

psoriasis

A
  • Psoriasis is a long-term skin condition that can also affect the nails and joints. It tends to flare up from time to time. (psoriatic arthritis- pitting, oncyholys = nail signs))
  • Increases risk of arthritis and CVD- inflammation of vasc
  • Subtypes
91
Q

plaque psoriasis

A

: the most common sub-type resulting in the typical well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp

92
Q

flexural psoriasis

A
  • : in contrast to plaque psoriasis the skin is smooth
93
Q

guttate psoriasis

A
  • transient psoriatic rash frequently triggered by a streptococcal infection. Multiple red, teardrop lesions appear on the body  trunk
94
Q

pustular psoriaiss

A

commonly occurs on palms and soles

95
Q

pathophysiology of psoriasis

A
  • Occurs due to increased production of skin cells
    • Skin cells normally replaced every 3-4 weeks, however in this chronic condition it only takes 3-7 days
    • Underlying cause not fully understood- to do with immune system mistaking healthy cells
96
Q

triggers of psoriasis

A
  • Injury to skin
  • Throat infection- step
  • Medications
  • Stress
  • Infection
  • Smoking andf alcohol
97
Q

presentation of psoriasis

A

Erythromatous, crusty skin covered with silvery scales

98
Q

management of psoriasis

A
  • Emollient
  • Corticosteroids
  • Vitamin D analogues
  • Salicylic acid (helping ointment peneatrate skin)
  • Tar preparations
  • Second line
    • Phototherapy (UV B)
    • DMARDs e.g. TNF antagonist adalimumab
99
Q

fir tree- pityriasis rosea

A

GP block (Y3) (39 decks)

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